Rheumatic diseases clinics of North America
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The office management of fibromyalgia (FM) is best determined by two variables: (1) the severity and complexity of each patient's symptoms, and (2) the specialization and interest of the treating physician. Because there are 6 to 10 million Americans with FM, most patient visits will be to the primary care physician. Rheumatologists, physiatrists, and other musculoskeletal specialists must work with primary care physicians to foster the early diagnosis and appropriate treatment of FM. ⋯ Rheumatologists should also assume the responsibility for the management of FM patients who have not responded to basic FM management. Additionally, some rheumatologists may wish to subspecialize in FM, a major career commitment to this perplexing disorder. These situations constitute advanced FM management.
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Rheum. Dis. Clin. North Am. · May 2002
ReviewThe promise of N-methyl-D-aspartate receptor antagonists in fibromyalgia.
There is strong evidence that intravenous administration of ketamine following a standardized protocol could be used as a diagnostic test for a central sensitization in the central nervous system in patients with FM. The combination of a weak opioid and an NMDA-receptor antagonist with few side effects is presently a promise for treatment of pain in a subgroup of patients with FM. The response to intravenously administered ketamine may help select patients for this treatment modality.
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Rheum. Dis. Clin. North Am. · May 2002
ReviewManagement of peripheral pain generators in fibromyalgia.
Fibromyalgia is a widespread chronic pain disorder that is characterized in part by central sensitization and increased pain response to peripheral nociceptive and non-nociceptive stimuli. Part of the comprehensive pain management of patients with fibromyalgia should include a thoughtful evaluation and search for peripheral pain generators that either are associated with fibromyalgia or are coincidentally present. The identification and treatment of these pain generators lessens the total pain burden, facilitates rehabilitation and decreases the stimuli for ongoing central sensitization.
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The two principal aims in the treatment of Wegener's granulomatosis (WG) are to limit the extent and severity of permanent organ damage by controlling the disease promptly and to minimize the short- and long-term morbidity that often results from therapy. Remission is considered to be the absence of disease activity in any organ system. Once the disease has been controlled by the initial treatment regimen, which is dictated by the degree of disease severity, the focus of therapy shifts to maintaining disease remission, often with medications less toxic than those used to induce remission. The description of WG treatments in terms analogous to cancer chemotherapy (i.e., those designed to induce remissions and those intended to maintain them) is useful in the formulation of current disease management strategies and in the investigation of new therapies for WG.
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Rheum. Dis. Clin. North Am. · Nov 2000
ReviewNeuroendocrine perturbations in fibromyalgia and chronic fatigue syndrome.
A large body of data from a number of different laboratories worldwide has demonstrated a general tendency for reduced adrenocortical responsiveness in CFS. It is still not clear if this is secondary to CNS abnormalities leading to decreased activity of CRH- or AVP-producing hypothalamic neurons. Primary hypofunction of the CRH neurons has been described on the basis of genetic and environmental influences. ⋯ Serotonin (5-HT) precursors such as tryptophan (5-HTP), drugs that release 5-HT, or drugs that act directly on 5-HT receptors stimulate the HPA axis, indicating a stimulatory effect of serotonergic input on HPA axis function. Hyperfunction of the HPA axis could also reflect an elevated serotonergic tonus in the CNS of FMS patients. The authors conclude that the observed pattern of hormonal deviations in patients with FMS is a CNS adjustment to chronic pain and stress, constitutes a specific entity of FMS, and is primarily evoked by activated CRH neurons.